Post cardiac arrest syndrome | Colombian Journal of Anesthesiology

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Tel.: +57 3406593." ] ] ] ] "titulosAlternativos" => array:1 [ "es" => array:1 [ "titulo" => "Síndrome posparo cardiaco" ] ] "textoCompleto" => "IntroductionIn 1972 the Russian pathophysiologist Vladimir Negovsky described the syndrome as “a post-resuscitation disease”.<a class="elsevierStyleCrossRef" href="#bib0005">1</a> However, since it involves a series of uncontrolled events, the International Liaison Committee on Resuscitation (ILCOR) adopted the term post cardiac arrest syndrome.<a class="elsevierStyleCrossRef" href="#bib0010">2</a>The incidence rate due to all cardiac causes is 460,000 deaths/year.<a class="elsevierStyleCrossRefs" href="#bib0015">3,4</a> Prospective trials refer to 350,000 coronary disease-related deaths/year; this is 1–2/1000 people for the American population.<a class="elsevierStyleCrossRef" href="#bib0025">5</a> There are survival reports of patients with extra-hospital cardiac arrest of 23.8% at the time of admission and of 7.6% at the time of discharge.<a class="elsevierStyleCrossRef" href="#bib0030">6</a>Biological death depends on the cardiac arrest mechanism, on the underlying disease and on the delay in starting the resuscitation maneuvers (CPR). A poor neurological prognosis after 4–6min of an unattended arrest is irreversible,<a class="elsevierStyleCrossRef" href="#bib0035">7</a> and hence resuscitation must be a constant mission.<a class="elsevierStyleCrossRef" href="#bib0040">8</a>When the arrest mechanism is an asystole or a pulseless electrical activity (PEA), the progression to neurological injury is faster and leads to a worse prognosis.<a class="elsevierStyleCrossRef" href="#bib0035">7</a>Mild therapeutic hypothermia (32–34°C) is the gold standard in post-arrest care.<a class="elsevierStyleCrossRef" href="#bib0045">9</a>A narrative review of the literature using Medline via PubMed and Clinical Trials using the terms MeSH cardiac arrest – Cardiopulmonary Resuscitation and no term MeSH Post cardiac arrest syndrome was carried out.Clinical evolutionOnce the patient recovers spontaneous cardiac circulation, a cascade of events develops, mainly characterized by anoxic brain injury, post cardiac arrest myocardial dysfunction, “ischemic/reperfusion” systemic response, and the typical pathology of the triggering cause of the cardiac arrest. The clinical evolution shall be dependent on clinical conditions such as the patient's co-morbidities, the duration of the ischemic lesion and the cause that triggered the cardiac arrest.<a class="elsevierStyleCrossRef" href="#bib0050">10</a>PathophysiologyOxygen deficiency and generalized acidosis develop during cardiac arrest. If the victim is resuscitated using CPR/defibrillation maneuvers, with resumption of spontaneous circulation, PCSS develops, which is characterized by a systemic inflammatory response of the immune system and of coagulation.<a class="elsevierStyleCrossRef" href="#bib0055">11</a> Cell damage seems to affect the enzyme calpain and peroxidation caused by oxygen free radicals that begin to develop during the phase of global ischemia and perpetuates during reperfusion.<a class="elsevierStyleCrossRef" href="#bib0060">12</a>The main cause of extra-hospital cardiac arrest in the adult is acute myocardial infarction.<a class="elsevierStyleCrossRef" href="#bib0065">13</a> There are many other pathologies leading to multisystem failure and subsequent cardiac arrest in the hospitalized patient.<a class="elsevierStyleCrossRef" href="#bib0065">13</a>TreatmentAccording to the ILCOR<a class="elsevierStyleCrossRefs" href="#bib0010">2,10</a> document, the PCAS classification follows physiological criteria in five phases:<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005">1.Immediate care: the initial 20min following the patient's spontaneous recovery of circulation.</li><li class="elsevierStyleListItem" id="lsti0010">2.Early phase: from 20min to 6–12h, when critical protective and therapeutic measures are required for a successful outcome.</li><li class="elsevierStyleListItem" id="lsti0015">3.Intermediate phase: from 6–12h to 72h a close surveillance and ICU treatment are required consistent with the therapeutic objectives.</li><li class="elsevierStyleListItem" id="lsti0020">4.Recovery phase: comprises the patient's condition after the initial 72h when there is a clearer diagnosis and a more predictable result.</li><li class="elsevierStyleListItem" id="lsti0025">5.Rehabilitation phase: focuses on the patient's complete recovery. Any electrolytic abnormalities shall be corrected during phases 1 and 2, in addition to providing inotropic support and optimized oxygenation.<a class="elsevierStyleCrossRef" href="#bib0070">14</a></li></ul>Goal-targeted therapyVentilation support<ul class="elsevierStyleList" id="lis0010"><li class="elsevierStyleListItem" id="lsti0030">1.Normocapnia (PaCO2 between 40 and 45mmHg). However, arterial gasometry should be properly interpreted in patients undergoing therapeutic hypothermia. When a patient reaches a central body temperature of close to 33°C, the actual PaCO2 may be up to 7mmHg below the value in the arterial gases machine.<a class="elsevierStyleCrossRef" href="#bib0075">15</a> Hyperventilation has been associated with a drop in coronary perfusion and venous return, in addition to cerebral vasoconstriction.<a class="elsevierStyleCrossRef" href="#bib0080">16</a></li><li class="elsevierStyleListItem" id="lsti0035">2.Normoxia. Both, hypoxia and hyperoxia (PaO2>300mmHg) may result in secondary neurological injury. Using an inspired oxygen fraction to maintain the arterial saturation between 95% and 99% or a PaO2>100mmHg is considered very reasonable.<a class="elsevierStyleCrossRef" href="#bib0085">17</a> However, other authors have not achieved similar results.<a class="elsevierStyleCrossRef" href="#bib0090">18</a></li></ul>Hemodynamic supportSystemic perfusion and in particular cerebral perfusion have prognostic implications. Cardiac arrest patients experience a loss of cerebral self-regulation. Based on positron emission tomography studies, the suggestion is to maintain a mean pressure between 80 and 100mmHg because this is the range in which perfusion matches the cerebral metabolic activity.<a class="elsevierStyleCrossRef" href="#bib0095">19</a> During the first 48–72h following the cardiac arrest, vasopressors and inotropic agents are usually needed. Transthoracic echocardiography may assist in accomplishing this goal. Apparently there is no difference in terms of the clinical prognosis regardless of the vasopressor (norepinephrine versus dopamine). Monitoring the mixed venous saturation may help in the interpretation of pharmacological interventions such as the introduction of inotropic agents.<a class="elsevierStyleCrossRef" href="#bib0100">20</a>Hypothermia has shown huge benefits since 2002;<a class="elsevierStyleCrossRefs" href="#bib0105">21,22</a> however, the procedure is not standardized in every country. There is an Italian study in ICUs indicating that only 16% used the therapeutic hypothermia protocol.<a class="elsevierStyleCrossRef" href="#bib0115">23</a>Hypothermia Management Scheme<a class="elsevierStyleCrossRef" href="#bib0120">24</a><ul class="elsevierStyleList" id="lis0015"><li class="elsevierStyleListItem" id="lsti0040">1.The induction phase (body temperature between 32°C and 34°C). It should be started early to prevent neuro-excitotoxicity.<a class="elsevierStyleCrossRef" href="#bib0125">25</a> It has been shown that the benefit of hypothermia will not be achieved if it is introduced after 6h of the spontaneous return of circulation.<a class="elsevierStyleCrossRef" href="#bib0130">26</a> Both PRINCE (Pre-ROSC Intranasal Cooling Effectiveness)<a class="elsevierStyleCrossRef" href="#bib0135">27</a> and Nagao<a class="elsevierStyleCrossRef" href="#bib0140">28</a> trials showed that initiating hypothermia before the patient recovers spontaneous cardiac circulation during CPR improves the neurological results and protects the myocardium from reperfusion injuries. Therapeutic hypothermia may not last less than 6h and it should be continued for 12–24h.<a class="elsevierStyleCrossRef" href="#bib0145">29</a>Some recommend starting a rapid saline solution infusion at 4°C to accomplish these goals.<a class="elsevierStyleCrossRef" href="#bib0150">30</a> The rate at which the body temperature drops is close to 1°C in 15min, when administering 1 liter of cold saline solution. This method is thought to be comparable to or even better than the use of intravascular catheters.<a class="elsevierStyleCrossRef" href="#bib0155">31</a> The infusion of 30ml/kg of saline solution at 4°C lowers the body temperature at a rate of over 2°C/h.<a class="elsevierStyleCrossRefs" href="#bib0150">30,32</a> Chills are one of the side effects of cooling down because of the rise in metabolic oxygen consumption; the recommendation to prevent chills includes administering magnesium sulfate (5g/5h), sedation and proper analgesia, in addition to the occasional administration of muscle relaxants.<a class="elsevierStyleCrossRefs" href="#bib0065">13,24</a> A very common intravenous sedation regime is titrating with a continuous infusion of Propofol (up to 50μg/kg/min) and Fentanyl. Hypothermia between 32°C and 34°C results in a drop in cardiac output (between 25% and 40%) at the expense of a heart rate decrease. Arrhythmias occur at much lower temperatures than these ranges or as a result of electrolyte imbalances.<a class="elsevierStyleCrossRef" href="#bib0120">24</a> The most destabilizing factors during this phase are hypovolemia and electrolyte imbalances (hypokalemia and hypomagnesemia). Increased diuresis results in a hydro-electrolytic imbalance, hemoconcentration and a rise in blood viscosity.<a class="elsevierStyleCrossRef" href="#bib0165">33</a></li><li class="elsevierStyleListItem" id="lsti0045">2.The maintenance phase should be free of any temperature variations beyond 0.2–0.5 degrees centigrade of the temperature achieved. Be very careful with the metabolic requirements of the patient since these are reduced in up to 50% and monitor coagulation, although different trials do not show a significant risk of bleeding.<a class="elsevierStyleCrossRefs" href="#bib0120">24,34</a> Hypothermia extends the half-life of all drugs. The administration of muscle relaxants may suppress chills and hence prevent rises in body temperature. However, muscle relaxants may mask seizures (that are present in up to 44% of the cases).<a class="elsevierStyleCrossRef" href="#bib0175">35</a> The therapeutic approach includes the use of multiple anti-convulsive agents as is the case in status epilepticus (valproic acid, phenytoin, midazolam, phenobarbital and propofol) because seizures tend to be refractory.<a class="elsevierStyleCrossRef" href="#bib0180">36</a></li><li class="elsevierStyleListItem" id="lsti0050">3.The premise during the warm-up phase is to slowly recover the temperature at a rate of 0.2–0.3 degrees centigrade. It is recommended to start warming-up after 12–24h of introducing the hypothermia until the temperature is normalized.<a class="elsevierStyleCrossRefs" href="#bib0065">13,24</a> It is usual to experience hyperkalemia, cerebral edema, and seizures during this phase; likewise, ruling out any risk of infection is a priority since one of the effects of hypothermia is the inhibition of the immune response. The use of antibiotic prophylaxis is only indicated for high-risk patients or in prolonged hypothermia (over 48h).<a class="elsevierStyleCrossRef" href="#bib0185">37</a> The level of coagulopathy is considered to be mild when compared against that of cardiac arrest victims who are maintained at a normal temperature.<a class="elsevierStyleCrossRef" href="#bib0190">38</a> Increased infection rates have been described associated with therapeutic hypothermia for 24h; however, it has not been associated with higher mortality.<a class="elsevierStyleCrossRefs" href="#bib0175">35,39</a> There can also be bradycardia, prolongation of the QTc segment, hyperglycemia, diuresis with subsequent hypokalemia, hypomagnesemia and hypofosfatemia.<a class="elsevierStyleCrossRef" href="#bib0195">39</a></li></ul>Hypothermia protectionDuring the first phase, when the patient recovers spontaneous circulation, hypothermia reduces the metabolic consumption of oxygen and glucose.<a class="elsevierStyleCrossRef" href="#bib0200">40</a>During the second phase, hypothermia reduces the occurrence of excitatory amino acids, particularly glutamate; these amino acids are responsible for the activation of the cytotoxic cascade, the formation of reactive oxygen species (ROS) and nitric oxide.During the third phase, hypothermia preserves the integrity of cell membranes interfering with the action of calpain and thus preventing the occurrence of cerebral edema, neuronal death and blood brain barrier injury.<a class="elsevierStyleCrossRefs" href="#bib0205">41–43</a><ul class="elsevierStyleList" id="lis0020"><li class="elsevierStyleListItem" id="lsti0055">The benefits of therapeutic hypothermia have been very well explained in a recent meta-analysis. Patients treated with therapeutic hypothermia exhibited improved neurological function (RR 1.55; 95 CI 1.22–1.96) and had a higher probability of survival at discharge (RR 1.35; 95 CI 1.10–1.65) compared to patients not treated with hypothermia.<a class="elsevierStyleCrossRef" href="#bib0220">44</a></li><li class="elsevierStyleListItem" id="lsti0060">The international agencies (AHA – ERC) have accepted and promoted the indication of hypothermia for managing the post cardiac arrest syndrome, not only in defibrillator-amenable patients, but also in cases of worse AESP prognosis and asystole in which the most important prognostic factor is the initiation of therapy.<a class="elsevierStyleCrossRefs" href="#bib0080">16,29</a></li><li class="elsevierStyleListItem" id="lsti0065">Indications for therapeutic hypothermia<a class="elsevierStyleCrossRefs" href="#bib0080">16,45</a><ul class="elsevierStyleList" id="lis0025"><li class="elsevierStyleListItem" id="lsti0070">Return to spontaneous cardiac circulation following cardiac arrest (any type of rhythm)</li><li class="elsevierStyleListItem" id="lsti0075">Coma</li><li class="elsevierStyleListItem" id="lsti0080">Over 18 years old</li></ul></li><li class="elsevierStyleListItem" id="lsti0085">Absolute contraindications<ul class="elsevierStyleList" id="lis0030"><li class="elsevierStyleListItem" id="lsti0090">Non-compressible active bleeding</li><li class="elsevierStyleListItem" id="lsti0095">Do not resuscitate medical order (DNR)</li></ul></li></ul>The hypothermia protocol must be interrupted in the presence of sepsis or pneumonia, refractory hemodynamic instability and severe refractory arrhythmia.Hypothermia in patients with a FV cardiac arrest has an NNT of 6 (confidence interval of 4–13). Despite the consistency of the trials in terms of the rhythm of presentation of the arrest, cooling method used, time to reach therapeutic hypothermia and duration thereof, no follow-up studies have been made beyond one year to establish the final neurological involvement.<a class="elsevierStyleCrossRef" href="#bib0230">46</a>Hypothermia should not be delayed, even when the patient requires transluminal percutaneous coronary angioplasty.<a class="elsevierStyleCrossRef" href="#bib0235">47</a>The best site to monitor the central temperature is through the pulmonary artery catheter or the central venous line; however, other sites are recommended such as the esophagus and the bladder, because they are easy to place and have minimal effects.<a class="elsevierStyleCrossRefs" href="#bib0065">13,48</a> The bladder temperature may be misinterpreted in the presence of oliguria.When should you do percutaneous coronary intervention (PCI) and thrombolysisAsk about any history of coronary heart disease, prior chest pain symptoms and initial arrest rhythm (if the QRS tracing in the ECG is widened, it is most likely of coronary etiology); however, the literature has not found a positive predictive value for coronary obstruction of these two parameters.<a class="elsevierStyleCrossRef" href="#bib0245">49</a>Thrombolysis is only recommended in isolated cases of pulmonary embolism and acute myocardial infarction with ST elevation (IAMST) and a 3-h therapeutic window or in the case of IAMST, with no other option for invasive coronary intervention.<a class="elsevierStyleCrossRef" href="#bib0250">50</a>In cardiac arrest patients with no evident extra cardiac cause or who present ST elevation in the ECG or sudden left branch blockade, an early angiographic exploration is recommended, followed by percutaneous coronary intervention.<a class="elsevierStyleCrossRef" href="#bib0250">50</a> In a report written by Spaulding et al.,<a class="elsevierStyleCrossRef" href="#bib0255">51</a> 49% of all cardiac arrest survivors who underwent routine coronary angiography showed a severe coronary obstruction.Further randomized clinical trials are needed showing the positive impact of emergency percutaneous coronary intervention in this syndrome. As of now, the studies reporting benefits with the use of PCI-associated therapeutic hypothermia exhibit various biases and undetermined confounding factors.<a class="elsevierStyleCrossRef" href="#bib0260">52</a>The similarity of the cardiohemic involvement of PCAS<a class="elsevierStyleCrossRef" href="#bib0165">33</a> to septic shock has led to the search of alternative aggressive management options with quite successful results such as circulatory support with extracorporeal oxygenation<a class="elsevierStyleCrossRef" href="#bib0265">53</a> and renal replacement therapy with high volume hemofiltration.<a class="elsevierStyleCrossRef" href="#bib0270">54</a>In refractory cardiac arrest patients, the alternative to use venous-arterial extracorporeal membrane oxygenation and PCI has been suggested.<a class="elsevierStyleCrossRef" href="#bib0260">52</a>Recommendation for neurological follow-up of the patientThe brain is the key organ in resuscitation, hence the high importance given to therapeutic hypothermia.<a class="elsevierStyleCrossRef" href="#bib0275">55</a> There is an interesting article on the “self-fulfilling prophecy”<a class="elsevierStyleCrossRef" href="#bib0280">56</a> that states that no negative prior judgments should be made in a patient who has overcome the arrest, regardless of the cause because by not doing what should be done, the patient will not survive, giving the false impression that what is appropriate is not to start any medical intervention under these circumstances. However, there is always room for uncertainty in every prognosis.<a class="elsevierStyleCrossRef" href="#bib0280">56</a>The prognosis after the clinical and paraclinical exams at different points in the evolution must have a 72-h (3 days) period of observation before any decision is made.<a class="elsevierStyleCrossRef" href="#bib0285">57</a> The American Academy of Neurology suggests that in the absence of brain death, findings of the clinical examination such as absence of corneal or pupillary reflexes, of motor response or extended absence of motor response, lead to a high rate or poor prognosis and consequently low false positives.<a class="elsevierStyleCrossRef" href="#bib0290">58</a>Efforts have been made to identify serum markers for predicting the development of multiple organ failure in PCAS patients. Soluble Ang1 factor stabilizes the endothelium Ang2 levels, and a higher proportion of Ang2/Ang1 is predictive of multiple organ failure and poor prognosis.<a class="elsevierStyleCrossRef" href="#bib0295">59</a>High procalcitonin levels are shown to be associated with PCAS and adverse neurological prognosis rather than to early infection in patients with anoxic encephalopathy.<a class="elsevierStyleCrossRef" href="#bib0300">60</a> Among the clinical factors themselves, a research comparing two hospitals in distant geographical regions showed that the pre- and intra-cardiac arrest conditions determine the severity of the PCAS.<a class="elsevierStyleCrossRef" href="#bib0305">61</a>Prognostic factors<a class="elsevierStyleCrossRef" href="#bib0065">13</a><ul class="elsevierStyleList" id="lis0035"><li class="elsevierStyleListItem" id="lsti0100">-Patient history: old age – diabetes – sepsis – CVA</li><li class="elsevierStyleListItem" id="lsti0105">-Cardiac arrest and resuscitation conditions: time elapsed since the cardiac arrest and the start of CPR – CPR quality – asystole as arrest rhythm – implementation of a protocol for managing the PCAS.<a class="elsevierStyleCrossRef" href="#bib0310">62</a></li><li class="elsevierStyleListItem" id="lsti0110">-Later evolution in accordance with the neurological examination, neurophysiological exams, neuroimaging, biochemical markers and intracranial Doppler.</li></ul>The two scales used to establish the degree of disability and the quality of life are the Glasgow prognostic scale<a class="elsevierStyleCrossRef" href="#bib0065">13</a> and the Glasgow-Pittsburgh<a class="elsevierStyleCrossRef" href="#bib0065">13</a> scale for categorizing brain performance.What is currently being done?A large international prospective trial was completed coordinated from Sweden<a class="elsevierStyleCrossRef" href="#bib0315">63</a> – the TTM trial (Target Temperature Management, identified as <a id="intr0005" class="elsevierStyleInterRef" href="https://clinicaltrials.gov/NCT01020916">NCT01020916</a>), whose results were published late in 2013. The purpose of the trial was to establish the level of evidence of hypothermia for the management of PCAS with optimal control to avoid hyperthermia in both groups; n: 939 adult patients. Comparison: controlled hypothermia (33°C) versus patients maintained with a temperature of 36°C. Period of time during which the patients were evaluated: up to 180 days. The results obtained are controversial with regard to the optimal threshold of hypothermia. The conclusion of the trial was based on a strict temperature control (below 36°C) to prevent hyperthermia, which is considered a determining factor for poor prognosis.<a class="elsevierStyleCrossRef" href="#bib0320">64</a> Emphasis was also placed on the establishment of standardized protocols, even for each subgroup of patients who may benefit from individualized treatment.<a class="elsevierStyleCrossRef" href="#bib0325">65</a>The recommendation is to optimize the perfusion of vital organs in addition to the brain, since the prevalence of multiple extra-cerebral organ failure impacts mortality, particularly the involvement of the cardiovascular (depends on the fine vasopressor support) and respiratory system (by providing improved oxygenation). An independent association has been identified between these two organs and their involvement has been linked to a higher hospital mortality in PCAS.<a class="elsevierStyleCrossRef" href="#bib0330">66</a>ConclusionPCAS is an entity that has been recognized for the last 40 years; however, the treatment for PCAS has only been established in an organized manner in the last decade.The pathophysiology includes a serious involvement of the brain and leads to myocardial dysfunction and systemic inflammation. Failure to intervene early on results in irreversible brain injury, vegetative state and death.FundingAuthors.Conflicts of interestThe authors have no conflicts of interest to declare." "textoCompletoSecciones" => array:1 [ "secciones" => array:15 [ 0 => array:2 [ "identificador" => "xres329752" "titulo" => array:6 [ 0 => "Abstract" 1 => "Background" 2 => "Objective" 3 => "Methodology" 4 => "Results" 5 => "Conclusions" ] ] 1 => array:2 [ "identificador" => "xpalclavsec311632" "titulo" => "Keywords" ] 2 => array:2 [ "identificador" => "xres329753" "titulo" => array:6 [ 0 => "Resumen" 1 => "Antecedentes" 2 => "Objetivo" 3 => "Metodología" 4 => "Resultados" 5 => "Conclusiones" ] ] 3 => array:2 [ "identificador" => "xpalclavsec311631" "titulo" => "Palabras clave" ] 4 => array:2 [ "identificador" => "sec0005" "titulo" => "Introduction" ] 5 => array:2 [ "identificador" => "sec0010" "titulo" => "Clinical evolution" ] 6 => array:2 [ "identificador" => "sec0015" "titulo" => "Pathophysiology" ] 7 => array:3 [ "identificador" => "sec0020" "titulo" => "Treatment" "secciones" => array:3 [ 0 => array:3 [ "identificador" => "sec0025" "titulo" => "Goal-targeted therapy" "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0030" "titulo" => "Ventilation support" ] 1 => array:2 [ "identificador" => "sec0035" "titulo" => "Hemodynamic support" ] ] ] 1 => array:2 [ "identificador" => "sec0040" "titulo" => "Hypothermia Management Scheme" ] 2 => array:2 [ "identificador" => "sec0045" "titulo" => "Hypothermia protection" ] ] ] 8 => array:2 [ "identificador" => "sec0050" "titulo" => "When should you do percutaneous coronary intervention (PCI) and thrombolysis" ] 9 => array:3 [ "identificador" => "sec0055" "titulo" => "Recommendation for neurological follow-up of the patient" "secciones" => array:1 [ 0 => array:2 [ "identificador" => "sec0080" "titulo" => "Prognostic factors" ] ] ] 10 => array:2 [ "identificador" => "sec0060" "titulo" => "What is currently being done?" ] 11 => array:2 [ "identificador" => "sec0065" "titulo" => "Conclusion" ] 12 => array:2 [ "identificador" => "sec0070" "titulo" => "Funding" ] 13 => array:2 [ "identificador" => "sec0075" "titulo" => "Conflicts of interest" ] 14 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "fechaRecibido" => "2013-07-29" "fechaAceptado" => "2014-01-20" "PalabrasClave" => array:2 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec311632" "palabras" => array:5 [ 0 => "Heart arrest" 1 => "Cardiopulmonary resuscitation" 2 => "Percutaneous coronary intervention" 3 => "Hypothermia induced" 4 => "Blood Circulation" ] ] ] "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec311631" "palabras" => array:5 [ 0 => "Paro cardiaco" 1 => "Resucitación cardiopulmonar" 2 => "Intervención coronaria percutánea" 3 => "Hipotermia inducida" 4 => "Circulación sanguínea" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "en" => array:2 [ "titulo" => "Abstract" "resumen" => "BackgroundResuscitation from cardiac arrest with global ischemia restores spontaneous circulation in some patients; however, survival depends on many factors associated with post cardiac arrest syndrome. During the last ten years, the understanding and control of these factors have improved the prognosis in a subgroup of patients. ObjectiveTo describe the pathophysiology and current management of the post cardiac arrest syndrome (PCAS). MethodologyNarrative review of the literature using Medline via PubMed and Clinical Trials, using the terms MeSH cardiac arrest – Cardiopulmonary Resuscitation and (no term MeSH) Post cardiac arrest syndrome. ResultsClinical trials have established a set of management protocols and guidelines based on therapeutic objectives with survival rates exceeding 50% of the cardiac arrest victims. ConclusionsThe management of this syndrome has actually strengthened the last link in the survival chain by standardizing the evaluation and selection of cardiac arrest victims via a therapeutic hypothermia protocol and early percutaneous coronary intervention." ] "es" => array:2 [ "titulo" => "Resumen" "resumen" => "AntecedentesLa reanimación en el paro cardiaco con isquemia global logra restablecer la circulación espontánea en algunos pacientes; sin embargo, la sobrevida depende de muchos factores que explican el síndrome posparo cardiaco. El entendimiento y el control de estos factores durante la última década han logrado mejorar el pronóstico en un subgrupo de pacientes. ObjetivoDescribir la fisiopatología y el manejo actual del síndrome posparo cardiaco. MetodologíaRevisión narrativa de la literatura a través de las bases electrónicas de Medline vía PubMed y Ensayos Clínicos usando los términos MeSH Cardiac arrest – Cardiopulmonary Resuscitation y (el término no MeSH) Post cardiac arrest syndrome. ResultadosLos estudios clínicos han establecido una serie de protocolos y guías de manejo basadas en objetivos terapéuticos con tasas de sobrevida que superan el 50% de las víctimas de paro cardiaco. ConclusionesActualmente el manejo de este síndrome ha fortalecido el último eslabón dela cadena de supervivencia al estandarizar la evaluación y la selección de víctimas de paro cardiaco con un protocolo de hipotermia terapéutica e intervención coronaria percutánea precoz." ] ] "NotaPie" => array:1 [ 0 => array:2 [ "etiqueta" => "☆" "nota" => "Please cite this article as: Navarro-Vargas JR, Díaz JL. Síndrome posparo cardiaco. 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Review

Post cardiac arrest syndrome

Síndrome posparo cardiaco

José Ricardo Navarro-Vargasa,

Corresponding author

jrnavarrovargas@hotmail.com

Corresponding author at: Universidad Nacional de Colombia, Calle 42 22 29, Bogotá, DC 0571, Colombia. Tel.: +57 3406593.

, José Luis Díazb

a Associate Professor, School of Medicine, Universidad Nacional de Colombia, Colombia

b Assistant Professor, Department of Anesthesia and Critical Care, Mayo Clinic, FL, USA

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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Introduction</span><p id="par0005" class="elsevierStylePara elsevierViewall">In 1972 the Russian pathophysiologist Vladimir Negovsky described the syndrome as &#8220;a post-resuscitation disease&#8221;&#46;<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a> However&#44; since it involves a series of uncontrolled events&#44; the International Liaison Committee on Resuscitation &#40;ILCOR&#41; adopted the term post cardiac arrest syndrome&#46;<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">The incidence rate due to all cardiac causes is 460&#44;000 deaths&#47;year&#46;<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3&#44;4</span></a> Prospective trials refer to 350&#44;000 coronary disease-related deaths&#47;year&#59; this is 1&#8211;2&#47;1000 people for the American population&#46;<a class="elsevierStyleCrossRef" href="#bib0025"><span class="elsevierStyleSup">5</span></a> There are survival reports of patients with extra-hospital cardiac arrest of 23&#46;8&#37; at the time of admission and of 7&#46;6&#37; at the time of discharge&#46;<a class="elsevierStyleCrossRef" href="#bib0030"><span class="elsevierStyleSup">6</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">Biological death depends on the cardiac arrest mechanism&#44; on the underlying disease and on the delay in starting the resuscitation maneuvers &#40;CPR&#41;&#46; A poor neurological prognosis after 4&#8211;6<span class="elsevierStyleHsp" style=""></span>min of an unattended arrest is irreversible&#44;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a> and hence resuscitation must be a constant mission&#46;<a class="elsevierStyleCrossRef" href="#bib0040"><span class="elsevierStyleSup">8</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">When the arrest mechanism is an asystole or a pulseless electrical activity &#40;PEA&#41;&#44; the progression to neurological injury is faster and leads to a worse prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0035"><span class="elsevierStyleSup">7</span></a></p><p id="par0025" class="elsevierStylePara elsevierViewall">Mild therapeutic hypothermia &#40;32&#8211;34<span class="elsevierStyleHsp" style=""></span>&#176;C&#41; is the gold standard in post-arrest care&#46;<a class="elsevierStyleCrossRef" href="#bib0045"><span class="elsevierStyleSup">9</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">A narrative review of the literature using Medline via PubMed and Clinical Trials using the terms MeSH cardiac arrest &#8211; Cardiopulmonary Resuscitation and no term MeSH Post cardiac arrest syndrome was carried out&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Clinical evolution</span><p id="par0035" class="elsevierStylePara elsevierViewall">Once the patient recovers spontaneous cardiac circulation&#44; a cascade of events develops&#44; mainly characterized by anoxic brain injury&#44; post cardiac arrest myocardial dysfunction&#44; &#8220;ischemic&#47;reperfusion&#8221; systemic response&#44; and the typical pathology of the triggering cause of the cardiac arrest&#46; The clinical evolution shall be dependent on clinical conditions such as the patient&#39;s co-morbidities&#44; the duration of the ischemic lesion and the cause that triggered the cardiac arrest&#46;<a class="elsevierStyleCrossRef" href="#bib0050"><span class="elsevierStyleSup">10</span></a></p></span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Pathophysiology</span><p id="par0040" class="elsevierStylePara elsevierViewall">Oxygen deficiency and generalized acidosis develop during cardiac arrest&#46; If the victim is resuscitated using CPR&#47;defibrillation maneuvers&#44; with resumption of spontaneous circulation&#44; PCSS develops&#44; which is characterized by a systemic inflammatory response of the immune system and of coagulation&#46;<a class="elsevierStyleCrossRef" href="#bib0055"><span class="elsevierStyleSup">11</span></a> Cell damage seems to affect the enzyme calpain and peroxidation caused by oxygen free radicals that begin to develop during the phase of global ischemia and perpetuates during reperfusion&#46;<a class="elsevierStyleCrossRef" href="#bib0060"><span class="elsevierStyleSup">12</span></a></p><p id="par0045" class="elsevierStylePara elsevierViewall">The main cause of extra-hospital cardiac arrest in the adult is acute myocardial infarction&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> There are many other pathologies leading to multisystem failure and subsequent cardiac arrest in the hospitalized patient&#46;<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Treatment</span><p id="par0050" class="elsevierStylePara elsevierViewall">According to the ILCOR<a class="elsevierStyleCrossRefs" href="#bib0010"><span class="elsevierStyleSup">2&#44;10</span></a> document&#44; the PCAS classification follows physiological criteria in five phases&#58;<ul class="elsevierStyleList" id="lis0005"><li class="elsevierStyleListItem" id="lsti0005"><span class="elsevierStyleLabel">1&#46;</span><p id="par0055" class="elsevierStylePara elsevierViewall">Immediate care&#58; the initial 20<span class="elsevierStyleHsp" style=""></span>min following the patient&#39;s spontaneous recovery of circulation&#46;</p></li><li class="elsevierStyleListItem" id="lsti0010"><span class="elsevierStyleLabel">2&#46;</span><p id="par0060" class="elsevierStylePara elsevierViewall">Early phase&#58; from 20<span class="elsevierStyleHsp" style=""></span>min to 6&#8211;12<span class="elsevierStyleHsp" style=""></span>h&#44; when critical protective and therapeutic measures are required for a successful outcome&#46;</p></li><li class="elsevierStyleListItem" id="lsti0015"><span class="elsevierStyleLabel">3&#46;</span><p id="par0065" class="elsevierStylePara elsevierViewall">Intermediate phase&#58; from 6&#8211;12<span class="elsevierStyleHsp" style=""></span>h to 72<span class="elsevierStyleHsp" style=""></span>h a close surveillance and ICU treatment are required consistent with the therapeutic objectives&#46;</p></li><li class="elsevierStyleListItem" id="lsti0020"><span class="elsevierStyleLabel">4&#46;</span><p id="par0070" class="elsevierStylePara elsevierViewall">Recovery phase&#58; comprises the patient&#39;s condition after the initial 72<span class="elsevierStyleHsp" style=""></span>h when there is a clearer diagnosis and a more predictable result&#46;</p></li><li class="elsevierStyleListItem" id="lsti0025"><span class="elsevierStyleLabel">5&#46;</span><p id="par0075" class="elsevierStylePara elsevierViewall">Rehabilitation phase&#58; focuses on the patient&#39;s complete recovery&#46; Any electrolytic abnormalities shall be corrected during phases 1 and 2&#44; in addition to providing inotropic support and optimized oxygenation&#46;<a class="elsevierStyleCrossRef" href="#bib0070"><span class="elsevierStyleSup">14</span></a></p></li></ul></p><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Goal-targeted therapy</span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Ventilation support</span><p id="par0080" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="lis0010"><li class="elsevierStyleListItem" id="lsti0030"><span class="elsevierStyleLabel">1&#46;</span><p id="par0085" class="elsevierStylePara elsevierViewall">Normocapnia &#40;PaCO<span class="elsevierStyleInf">2</span> between 40 and 45<span class="elsevierStyleHsp" style=""></span>mmHg&#41;&#46; However&#44; arterial gasometry should be properly interpreted in patients undergoing therapeutic hypothermia&#46; When a patient reaches a central body temperature of close to 33<span class="elsevierStyleHsp" style=""></span>&#176;C&#44; the actual PaCO<span class="elsevierStyleInf">2</span> may be up to 7<span class="elsevierStyleHsp" style=""></span>mmHg below the value in the arterial gases machine&#46;<a class="elsevierStyleCrossRef" href="#bib0075"><span class="elsevierStyleSup">15</span></a> Hyperventilation has been associated with a drop in coronary perfusion and venous return&#44; in addition to cerebral vasoconstriction&#46;<a class="elsevierStyleCrossRef" href="#bib0080"><span class="elsevierStyleSup">16</span></a></p></li><li class="elsevierStyleListItem" id="lsti0035"><span class="elsevierStyleLabel">2&#46;</span><p id="par0090" class="elsevierStylePara elsevierViewall">Normoxia&#46; Both&#44; hypoxia and hyperoxia &#40;PaO<span class="elsevierStyleInf">2</span><span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>300<span class="elsevierStyleHsp" style=""></span>mmHg&#41; may result in secondary neurological injury&#46; Using an inspired oxygen fraction to maintain the arterial saturation between 95&#37; and 99&#37; or a PaO<span class="elsevierStyleInf">2</span><span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>100<span class="elsevierStyleHsp" style=""></span>mmHg is considered very reasonable&#46;<a class="elsevierStyleCrossRef" href="#bib0085"><span class="elsevierStyleSup">17</span></a> However&#44; other authors have not achieved similar results&#46;<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">18</span></a></p></li></ul></p></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Hemodynamic support</span><p id="par0095" class="elsevierStylePara elsevierViewall">Systemic perfusion and in particular cerebral perfusion have prognostic implications&#46; Cardiac arrest patients experience a loss of cerebral self-regulation&#46; Based on positron emission tomography studies&#44; the suggestion is to maintain a mean pressure between 80 and 100<span class="elsevierStyleHsp" style=""></span>mmHg because this is the range in which perfusion matches the cerebral metabolic activity&#46;<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">19</span></a> During the first 48&#8211;72<span class="elsevierStyleHsp" style=""></span>h following the cardiac arrest&#44; vasopressors and inotropic agents are usually needed&#46; Transthoracic echocardiography may assist in accomplishing this goal&#46; Apparently there is no difference in terms of the clinical prognosis regardless of the vasopressor &#40;norepinephrine versus dopamine&#41;&#46; Monitoring the mixed venous saturation may help in the interpretation of pharmacological interventions such as the introduction of inotropic agents&#46;<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">20</span></a></p><p id="par0100" class="elsevierStylePara elsevierViewall">Hypothermia has shown huge benefits since 2002&#59;<a class="elsevierStyleCrossRefs" href="#bib0105"><span class="elsevierStyleSup">21&#44;22</span></a> however&#44; the procedure is not standardized in every country&#46; There is an Italian study in ICUs indicating that only 16&#37; used the therapeutic hypothermia protocol&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">23</span></a></p></span></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Hypothermia Management Scheme<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a></span><p id="par0105" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="lis0015"><li class="elsevierStyleListItem" id="lsti0040"><span class="elsevierStyleLabel">1&#46;</span><p id="par0110" class="elsevierStylePara elsevierViewall">The induction phase &#40;body temperature between 32<span class="elsevierStyleHsp" style=""></span>&#176;C and 34<span class="elsevierStyleHsp" style=""></span>&#176;C&#41;&#46; It should be started early to prevent neuro-excitotoxicity&#46;<a class="elsevierStyleCrossRef" href="#bib0125"><span class="elsevierStyleSup">25</span></a> It has been shown that the benefit of hypothermia will not be achieved if it is introduced after 6<span class="elsevierStyleHsp" style=""></span>h of the spontaneous return of circulation&#46;<a class="elsevierStyleCrossRef" href="#bib0130"><span class="elsevierStyleSup">26</span></a> Both PRINCE &#40;Pre-ROSC Intranasal Cooling Effectiveness&#41;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">27</span></a> and Nagao<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">28</span></a> trials showed that initiating hypothermia before the patient recovers spontaneous cardiac circulation during CPR improves the neurological results and protects the myocardium from reperfusion injuries&#46; Therapeutic hypothermia may not last less than 6<span class="elsevierStyleHsp" style=""></span>h and it should be continued for 12&#8211;24<span class="elsevierStyleHsp" style=""></span>h&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">29</span></a></p><p id="par0115" class="elsevierStylePara elsevierViewall">Some recommend starting a rapid saline solution infusion at 4<span class="elsevierStyleHsp" style=""></span>&#176;C to accomplish these goals&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">30</span></a> The rate at which the body temperature drops is close to 1<span class="elsevierStyleHsp" style=""></span>&#176;C in 15<span class="elsevierStyleHsp" style=""></span>min&#44; when administering 1 liter of cold saline solution&#46; This method is thought to be comparable to or even better than the use of intravascular catheters&#46;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">31</span></a> The infusion of 30<span class="elsevierStyleHsp" style=""></span>ml&#47;kg of saline solution at 4<span class="elsevierStyleHsp" style=""></span>&#176;C lowers the body temperature at a rate of over 2<span class="elsevierStyleHsp" style=""></span>&#176;C&#47;h&#46;<a class="elsevierStyleCrossRefs" href="#bib0150"><span class="elsevierStyleSup">30&#44;32</span></a> Chills are one of the side effects of cooling down because of the rise in metabolic oxygen consumption&#59; the recommendation to prevent chills includes administering magnesium sulfate &#40;5<span class="elsevierStyleHsp" style=""></span>g&#47;5<span class="elsevierStyleHsp" style=""></span>h&#41;&#44; sedation and proper analgesia&#44; in addition to the occasional administration of muscle relaxants&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13&#44;24</span></a> A very common intravenous sedation regime is titrating with a continuous infusion of Propofol &#40;up to 50<span class="elsevierStyleHsp" style=""></span>&#956;g&#47;kg&#47;min&#41; and Fentanyl&#46; Hypothermia between 32<span class="elsevierStyleHsp" style=""></span>&#176;C and 34<span class="elsevierStyleHsp" style=""></span>&#176;C results in a drop in cardiac output &#40;between 25&#37; and 40&#37;&#41; at the expense of a heart rate decrease&#46; Arrhythmias occur at much lower temperatures than these ranges or as a result of electrolyte imbalances&#46;<a class="elsevierStyleCrossRef" href="#bib0120"><span class="elsevierStyleSup">24</span></a> The most destabilizing factors during this phase are hypovolemia and electrolyte imbalances &#40;hypokalemia and hypomagnesemia&#41;&#46; Increased diuresis results in a hydro-electrolytic imbalance&#44; hemoconcentration and a rise in blood viscosity&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a></p></li><li class="elsevierStyleListItem" id="lsti0045"><span class="elsevierStyleLabel">2&#46;</span><p id="par0120" class="elsevierStylePara elsevierViewall">The maintenance phase should be free of any temperature variations beyond 0&#46;2&#8211;0&#46;5 degrees centigrade of the temperature achieved&#46; Be very careful with the metabolic requirements of the patient since these are reduced in up to 50&#37; and monitor coagulation&#44; although different trials do not show a significant risk of bleeding&#46;<a class="elsevierStyleCrossRefs" href="#bib0120"><span class="elsevierStyleSup">24&#44;34</span></a> Hypothermia extends the half-life of all drugs&#46; The administration of muscle relaxants may suppress chills and hence prevent rises in body temperature&#46; However&#44; muscle relaxants may mask seizures &#40;that are present in up to 44&#37; of the cases&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0175"><span class="elsevierStyleSup">35</span></a> The therapeutic approach includes the use of multiple anti-convulsive agents as is the case in status epilepticus &#40;valproic acid&#44; phenytoin&#44; midazolam&#44; phenobarbital and propofol&#41; because seizures tend to be refractory&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">36</span></a></p></li><li class="elsevierStyleListItem" id="lsti0050"><span class="elsevierStyleLabel">3&#46;</span><p id="par0125" class="elsevierStylePara elsevierViewall">The premise during the warm-up phase is to slowly recover the temperature at a rate of 0&#46;2&#8211;0&#46;3 degrees centigrade&#46; It is recommended to start warming-up after 12&#8211;24<span class="elsevierStyleHsp" style=""></span>h of introducing the hypothermia until the temperature is normalized&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13&#44;24</span></a> It is usual to experience hyperkalemia&#44; cerebral edema&#44; and seizures during this phase&#59; likewise&#44; ruling out any risk of infection is a priority since one of the effects of hypothermia is the inhibition of the immune response&#46; The use of antibiotic prophylaxis is only indicated for high-risk patients or in prolonged hypothermia &#40;over 48<span class="elsevierStyleHsp" style=""></span>h&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0185"><span class="elsevierStyleSup">37</span></a> The level of coagulopathy is considered to be mild when compared against that of cardiac arrest victims who are maintained at a normal temperature&#46;<a class="elsevierStyleCrossRef" href="#bib0190"><span class="elsevierStyleSup">38</span></a> Increased infection rates have been described associated with therapeutic hypothermia for 24<span class="elsevierStyleHsp" style=""></span>h&#59; however&#44; it has not been associated with higher mortality&#46;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">35&#44;39</span></a> There can also be bradycardia&#44; prolongation of the QTc segment&#44; hyperglycemia&#44; diuresis with subsequent hypokalemia&#44; hypomagnesemia and hypofosfatemia&#46;<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">39</span></a></p></li></ul></p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Hypothermia protection</span><p id="par0130" class="elsevierStylePara elsevierViewall">During the first phase&#44; when the patient recovers spontaneous circulation&#44; hypothermia reduces the metabolic consumption of oxygen and glucose&#46;<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">40</span></a></p><p id="par0135" class="elsevierStylePara elsevierViewall">During the second phase&#44; hypothermia reduces the occurrence of excitatory amino acids&#44; particularly glutamate&#59; these amino acids are responsible for the activation of the cytotoxic cascade&#44; the formation of reactive oxygen species &#40;ROS&#41; and nitric oxide&#46;</p><p id="par0140" class="elsevierStylePara elsevierViewall">During the third phase&#44; hypothermia preserves the integrity of cell membranes interfering with the action of calpain and thus preventing the occurrence of cerebral edema&#44; neuronal death and blood brain barrier injury&#46;<a class="elsevierStyleCrossRefs" href="#bib0205"><span class="elsevierStyleSup">41&#8211;43</span></a><ul class="elsevierStyleList" id="lis0020"><li class="elsevierStyleListItem" id="lsti0055"><p id="par0145" class="elsevierStylePara elsevierViewall">The benefits of therapeutic hypothermia have been very well explained in a recent meta-analysis&#46; Patients treated with therapeutic hypothermia exhibited improved neurological function &#40;RR 1&#46;55&#59; 95 CI 1&#46;22&#8211;1&#46;96&#41; and had a higher probability of survival at discharge &#40;RR 1&#46;35&#59; 95 CI 1&#46;10&#8211;1&#46;65&#41; compared to patients not treated with hypothermia&#46;<a class="elsevierStyleCrossRef" href="#bib0220"><span class="elsevierStyleSup">44</span></a></p></li><li class="elsevierStyleListItem" id="lsti0060"><p id="par0150" class="elsevierStylePara elsevierViewall">The international agencies &#40;AHA &#8211; ERC&#41; have accepted and promoted the indication of hypothermia for managing the post cardiac arrest syndrome&#44; not only in defibrillator-amenable patients&#44; but also in cases of worse AESP prognosis and asystole in which the most important prognostic factor is the <span class="elsevierStyleItalic">initiation of therapy</span>&#46;<a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">16&#44;29</span></a></p></li><li class="elsevierStyleListItem" id="lsti0065"><p id="par0155" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Indications for therapeutic hypothermia</span><a class="elsevierStyleCrossRefs" href="#bib0080"><span class="elsevierStyleSup">16&#44;45</span></a><ul class="elsevierStyleList" id="lis0025"><li class="elsevierStyleListItem" id="lsti0070"><p id="par0160" class="elsevierStylePara elsevierViewall">Return to spontaneous cardiac circulation following cardiac arrest &#40;any type of rhythm&#41;</p></li><li class="elsevierStyleListItem" id="lsti0075"><p id="par0165" class="elsevierStylePara elsevierViewall">Coma</p></li><li class="elsevierStyleListItem" id="lsti0080"><p id="par0170" class="elsevierStylePara elsevierViewall">Over 18 years old</p></li></ul></p></li><li class="elsevierStyleListItem" id="lsti0085"><p id="par0175" class="elsevierStylePara elsevierViewall"><span class="elsevierStyleItalic">Absolute contraindications</span><ul class="elsevierStyleList" id="lis0030"><li class="elsevierStyleListItem" id="lsti0090"><p id="par0180" class="elsevierStylePara elsevierViewall">Non-compressible active bleeding</p></li><li class="elsevierStyleListItem" id="lsti0095"><p id="par0185" class="elsevierStylePara elsevierViewall">Do not resuscitate medical order &#40;DNR&#41;</p></li></ul></p></li></ul></p><p id="par0190" class="elsevierStylePara elsevierViewall">The hypothermia protocol must be interrupted in the presence of sepsis or pneumonia&#44; refractory hemodynamic instability and severe refractory arrhythmia&#46;</p><p id="par0195" class="elsevierStylePara elsevierViewall">Hypothermia in patients with a FV cardiac arrest has an NNT of 6 &#40;confidence interval of 4&#8211;13&#41;&#46; Despite the consistency of the trials in terms of the rhythm of presentation of the arrest&#44; cooling method used&#44; time to reach therapeutic hypothermia and duration thereof&#44; no follow-up studies have been made beyond one year to establish the final neurological involvement&#46;<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">46</span></a></p><p id="par0200" class="elsevierStylePara elsevierViewall">Hypothermia should not be delayed&#44; even when the patient requires transluminal percutaneous coronary angioplasty&#46;<a class="elsevierStyleCrossRef" href="#bib0235"><span class="elsevierStyleSup">47</span></a></p><p id="par0205" class="elsevierStylePara elsevierViewall">The best site to monitor the central temperature is through the pulmonary artery catheter or the central venous line&#59; however&#44; other sites are recommended such as the esophagus and the bladder&#44; because they are easy to place and have minimal effects&#46;<a class="elsevierStyleCrossRefs" href="#bib0065"><span class="elsevierStyleSup">13&#44;48</span></a> The bladder temperature may be misinterpreted in the presence of oliguria&#46;</p></span></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0120">When should you do percutaneous coronary intervention &#40;PCI&#41; and thrombolysis</span><p id="par0210" class="elsevierStylePara elsevierViewall">Ask about any history of coronary heart disease&#44; prior chest pain symptoms and initial arrest rhythm &#40;if the QRS tracing in the ECG is widened&#44; it is most likely of coronary etiology&#41;&#59; however&#44; the literature has not found a positive predictive value for coronary obstruction of these two parameters&#46;<a class="elsevierStyleCrossRef" href="#bib0245"><span class="elsevierStyleSup">49</span></a></p><p id="par0215" class="elsevierStylePara elsevierViewall">Thrombolysis is only recommended in isolated cases of pulmonary embolism and acute myocardial infarction with ST elevation &#40;IAMST&#41; and a 3-h therapeutic window or in the case of IAMST&#44; with no other option for invasive coronary intervention&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">50</span></a></p><p id="par0220" class="elsevierStylePara elsevierViewall">In cardiac arrest patients with no evident extra cardiac cause or who present ST elevation in the ECG or sudden left branch blockade&#44; an early angiographic exploration is recommended&#44; followed by percutaneous coronary intervention&#46;<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">50</span></a> In a report written by Spaulding et al&#46;&#44;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">51</span></a> 49&#37; of all cardiac arrest survivors who underwent routine coronary angiography showed a severe coronary obstruction&#46;</p><p id="par0225" class="elsevierStylePara elsevierViewall">Further randomized clinical trials are needed showing the positive impact of emergency percutaneous coronary intervention in this syndrome&#46; As of now&#44; the studies reporting benefits with the use of PCI-associated therapeutic hypothermia exhibit various biases and undetermined confounding factors&#46;<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a></p><p id="par0230" class="elsevierStylePara elsevierViewall">The similarity of the cardiohemic involvement of PCAS<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">33</span></a> to septic shock has led to the search of alternative aggressive management options with quite successful results such as circulatory support with extracorporeal oxygenation<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">53</span></a> and renal replacement therapy with high volume hemofiltration&#46;<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">54</span></a></p><p id="par0235" class="elsevierStylePara elsevierViewall">In refractory cardiac arrest patients&#44; the alternative to use venous-arterial extracorporeal membrane oxygenation and PCI has been suggested&#46;<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">52</span></a></p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0125">Recommendation for neurological follow-up of the patient</span><p id="par0240" class="elsevierStylePara elsevierViewall">The brain is the key organ in resuscitation&#44; hence the high importance given to therapeutic hypothermia&#46;<a class="elsevierStyleCrossRef" href="#bib0275"><span class="elsevierStyleSup">55</span></a> There is an interesting article on the &#8220;self-fulfilling prophecy&#8221;<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">56</span></a> that states that no negative prior judgments should be made in a patient who has overcome the arrest&#44; regardless of the cause because by not doing what should be done&#44; the patient will not survive&#44; giving the false impression that what is appropriate is not to start any medical intervention under these circumstances&#46; However&#44; there is always room for uncertainty in every prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0280"><span class="elsevierStyleSup">56</span></a></p><p id="par0245" class="elsevierStylePara elsevierViewall">The prognosis after the clinical and paraclinical exams at different points in the evolution must have a 72-h &#40;3 days&#41; period of observation before any decision is made&#46;<a class="elsevierStyleCrossRef" href="#bib0285"><span class="elsevierStyleSup">57</span></a> The American Academy of Neurology suggests that in the absence of brain death&#44; findings of the clinical examination such as absence of corneal or pupillary reflexes&#44; of motor response or extended absence of motor response&#44; lead to a high rate or poor prognosis and consequently low false positives&#46;<a class="elsevierStyleCrossRef" href="#bib0290"><span class="elsevierStyleSup">58</span></a></p><p id="par0250" class="elsevierStylePara elsevierViewall">Efforts have been made to identify serum markers for predicting the development of multiple organ failure in PCAS patients&#46; Soluble Ang1 factor stabilizes the endothelium Ang2 levels&#44; and a higher proportion of Ang2&#47;Ang1 is predictive of multiple organ failure and poor prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0295"><span class="elsevierStyleSup">59</span></a></p><p id="par0255" class="elsevierStylePara elsevierViewall">High procalcitonin levels are shown to be associated with PCAS and adverse neurological prognosis rather than to early infection in patients with anoxic encephalopathy&#46;<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">60</span></a> Among the clinical factors themselves&#44; a research comparing two hospitals in distant geographical regions showed that the pre- and intra-cardiac arrest conditions determine the severity of the PCAS&#46;<a class="elsevierStyleCrossRef" href="#bib0305"><span class="elsevierStyleSup">61</span></a></p><span id="sec0080" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0130">Prognostic factors<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a></span><p id="par0315" class="elsevierStylePara elsevierViewall"><ul class="elsevierStyleList" id="lis0035"><li class="elsevierStyleListItem" id="lsti0100"><span class="elsevierStyleLabel">-</span><p id="par0265" class="elsevierStylePara elsevierViewall">Patient history&#58; old age &#8211; diabetes &#8211; sepsis &#8211; CVA</p></li><li class="elsevierStyleListItem" id="lsti0105"><span class="elsevierStyleLabel">-</span><p id="par0270" class="elsevierStylePara elsevierViewall">Cardiac arrest and resuscitation conditions&#58; time elapsed since the cardiac arrest and the start of CPR &#8211; CPR quality &#8211; asystole as arrest rhythm &#8211; implementation of a protocol for managing the PCAS&#46;<a class="elsevierStyleCrossRef" href="#bib0310"><span class="elsevierStyleSup">62</span></a></p></li><li class="elsevierStyleListItem" id="lsti0110"><span class="elsevierStyleLabel">-</span><p id="par0275" class="elsevierStylePara elsevierViewall">Later evolution in accordance with the neurological examination&#44; neurophysiological exams&#44; neuroimaging&#44; biochemical markers and intracranial Doppler&#46;</p></li></ul></p><p id="par0280" class="elsevierStylePara elsevierViewall">The two scales used to establish the degree of disability and the quality of life are the Glasgow prognostic scale<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> and the Glasgow-Pittsburgh<a class="elsevierStyleCrossRef" href="#bib0065"><span class="elsevierStyleSup">13</span></a> scale for categorizing brain performance&#46;</p></span></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0135">What is currently being done&#63;</span><p id="par0285" class="elsevierStylePara elsevierViewall">A large international prospective trial was completed coordinated from Sweden<a class="elsevierStyleCrossRef" href="#bib0315"><span class="elsevierStyleSup">63</span></a> &#8211; the TTM trial &#40;Target Temperature Management&#44; identified as <a id="intr0005" class="elsevierStyleInterRef" href="https://clinicaltrials.gov/NCT01020916">NCT01020916</a>&#41;&#44; whose results were published late in 2013&#46; The purpose of the trial was to establish the level of evidence of hypothermia for the management of PCAS with optimal control to avoid hyperthermia in both groups&#59; <span class="elsevierStyleItalic">n</span>&#58; 939 adult patients&#46; Comparison&#58; controlled hypothermia &#40;33<span class="elsevierStyleHsp" style=""></span>&#176;C&#41; versus patients maintained with a temperature of 36<span class="elsevierStyleHsp" style=""></span>&#176;C&#46; Period of time during which the patients were evaluated&#58; up to 180 days&#46; The results obtained are controversial with regard to the optimal threshold of hypothermia&#46; The conclusion of the trial was based on a strict temperature control &#40;below 36<span class="elsevierStyleHsp" style=""></span>&#176;C&#41; to prevent hyperthermia&#44; which is considered a determining factor for poor prognosis&#46;<a class="elsevierStyleCrossRef" href="#bib0320"><span class="elsevierStyleSup">64</span></a> Emphasis was also placed on the establishment of standardized protocols&#44; even for each subgroup of patients who may benefit from individualized treatment&#46;<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">65</span></a></p><p id="par0290" class="elsevierStylePara elsevierViewall">The recommendation is to optimize the perfusion of vital organs in addition to the brain&#44; since the prevalence of multiple extra-cerebral organ failure impacts mortality&#44; particularly the involvement of the cardiovascular &#40;depends on the fine vasopressor support&#41; and respiratory system &#40;by providing improved oxygenation&#41;&#46; An independent association has been identified between these two organs and their involvement has been linked to a higher hospital mortality in PCAS&#46;<a class="elsevierStyleCrossRef" href="#bib0330"><span class="elsevierStyleSup">66</span></a></p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0140">Conclusion</span><p id="par0295" class="elsevierStylePara elsevierViewall">PCAS is an entity that has been recognized for the last 40 years&#59; however&#44; the treatment for PCAS has only been established in an organized manner in the last decade&#46;</p><p id="par0300" class="elsevierStylePara elsevierViewall">The pathophysiology includes a serious involvement of the brain and leads to myocardial dysfunction and systemic inflammation&#46; Failure to intervene early on results in irreversible brain injury&#44; vegetative state and death&#46;</p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0145">Funding</span><p id="par0305" class="elsevierStylePara elsevierViewall">Authors&#46;</p></span><span id="sec0075" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0150">Conflicts of interest</span><p id="par0310" class="elsevierStylePara elsevierViewall">The authors have no conflicts of interest to declare&#46;</p></span></span>"
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          "titulo" => "When should you do percutaneous coronary intervention &#40;PCI&#41; and thrombolysis"
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            2 => "Intervenci&#243;n coronaria percut&#225;nea"
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        "titulo" => "Abstract"
        "resumen" => "<span class="elsevierStyleSectionTitle" id="sect0010">Background</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Resuscitation from cardiac arrest with global ischemia restores spontaneous circulation in some patients&#59; however&#44; survival depends on many factors associated with post cardiac arrest syndrome&#46; During the last ten years&#44; the understanding and control of these factors have improved the prognosis in a subgroup of patients&#46;</p> <span class="elsevierStyleSectionTitle" id="sect0015">Objective</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">To describe the pathophysiology and current management of the post cardiac arrest syndrome &#40;PCAS&#41;&#46;</p> <span class="elsevierStyleSectionTitle" id="sect0020">Methodology</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Narrative review of the literature using Medline via PubMed and Clinical Trials&#44; using the terms MeSH cardiac arrest &#8211; Cardiopulmonary Resuscitation and &#40;no term MeSH&#41; Post cardiac arrest syndrome&#46;</p> <span class="elsevierStyleSectionTitle" id="sect0025">Results</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Clinical trials have established a set of management protocols and guidelines based on therapeutic objectives with survival rates exceeding 50&#37; of the cardiac arrest victims&#46;</p> <span class="elsevierStyleSectionTitle" id="sect0030">Conclusions</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">The management of this syndrome has actually strengthened the last link in the survival chain by standardizing the evaluation and selection of cardiac arrest victims via a therapeutic hypothermia protocol and early percutaneous coronary intervention&#46;</p>"
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        "resumen" => "<span class="elsevierStyleSectionTitle" id="sect0040">Antecedentes</span><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">La reanimaci&#243;n en el paro cardiaco con isquemia global logra restablecer la circulaci&#243;n espont&#225;nea en algunos pacientes&#59; sin embargo&#44; la sobrevida depende de muchos factores que explican el s&#237;ndrome posparo cardiaco&#46; El entendimiento y el control de estos factores durante la &#250;ltima d&#233;cada han logrado mejorar el pron&#243;stico en un subgrupo de pacientes&#46;</p> <span class="elsevierStyleSectionTitle" id="sect0045">Objetivo</span><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Describir la fisiopatolog&#237;a y el manejo actual del s&#237;ndrome posparo cardiaco&#46;</p> <span class="elsevierStyleSectionTitle" id="sect0050">Metodolog&#237;a</span><p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">Revisi&#243;n narrativa de la literatura a trav&#233;s de las bases electr&#243;nicas de Medline v&#237;a PubMed y Ensayos Cl&#237;nicos usando los t&#233;rminos MeSH <span class="elsevierStyleItalic">Cardiac arrest &#8211; Cardiopulmonary Resuscitation</span> y &#40;el t&#233;rmino no MeSH&#41; <span class="elsevierStyleItalic">Post cardiac arrest syndrome&#46;</span></p> <span class="elsevierStyleSectionTitle" id="sect0055">Resultados</span><p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Los estudios cl&#237;nicos han establecido una serie de protocolos y gu&#237;as de manejo basadas en objetivos terap&#233;uticos con tasas de sobrevida que superan el 50&#37; de las v&#237;ctimas de paro cardiaco&#46;</p> <span class="elsevierStyleSectionTitle" id="sect0060">Conclusiones</span><p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">Actualmente el manejo de este s&#237;ndrome ha fortalecido el &#250;ltimo eslab&#243;n dela cadena de supervivencia al estandarizar la evaluaci&#243;n y la selecci&#243;n de v&#237;ctimas de paro cardiaco con un protocolo de hipotermia terap&#233;utica e intervenci&#243;n coronaria percut&#225;nea precoz&#46;</p>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Please cite this article as&#58; Navarro-Vargas JR&#44; D&#237;az JL&#46; S&#237;ndrome posparo cardiaco&#46; Rev Colomb Anestesiol&#46; 2014&#59;42&#58;107&#8211;113&#46;</p>"
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Article information

ISSN: 22562087
Original language: English

DOI:10.1016/j.rcae.2014.01.004

The statistics are updated each day

Year/Month	Html	Pdf	Total

2024 November	3	0	3
2024 October	22	5	27
2024 September	42	4	46
2024 August	36	7	43
2024 July	34	12	46
2024 June	31	6	37
2024 May	26	6	32
2024 April	50	16	66
2024 March	83	21	104
2024 February	240	15	255
2024 January	44	19	63
2023 December	62	10	72
2023 November	64	21	85
2023 October	34	22	56
2023 September	46	13	59
2023 August	33	11	44
2023 July	33	15	48
2023 June	39	5	44
2023 May	92	15	107
2023 April	73	13	86
2023 March	69	16	85
2023 February	37	10	47
2023 January	23	16	39
2022 December	43	3	46
2022 November	33	7	40
2022 October	26	18	44
2022 September	21	10	31
2022 August	28	17	45
2022 July	21	10	31
2022 June	28	9	37
2022 May	17	27	44
2022 April	42	34	76
2022 March	84	26	110
2022 February	50	33	83
2022 January	42	22	64
2021 December	32	31	63
2021 November	52	22	74
2021 October	47	22	69
2021 September	37	16	53
2021 August	39	20	59
2021 July	33	28	61
2021 June	28	12	40
2021 May	53	16	69
2021 April	190	84	274
2021 March	206	83	289
2021 February	58	18	76
2021 January	55	16	71
2020 December	58	14	72
2020 November	66	10	76
2020 October	28	6	34
2020 September	40	21	61
2020 August	36	21	57
2020 July	16	5	21
2020 June	14	7	21
2020 May	14	7	21
2020 April	15	10	25
2020 March	23	21	44
2020 February	12	7	19
2020 January	22	4	26
2019 December	13	10	23
2019 November	5	6	11
2019 October	4	5	9
2019 September	5	0	5
2019 August	2	0	2
2019 July	6	12	18
2019 June	2	0	2
2019 May	1	10	11
2018 September	1	0	1
2018 August	0	1	1
2018 June	5	2	7
2018 May	31	12	43
2018 April	45	7	52
2018 March	24	7	31
2018 February	24	6	30
2018 January	49	6	55
2017 December	35	6	41
2017 November	41	8	49
2017 October	36	9	45
2017 September	54	9	63
2017 August	59	7	66
2017 July	55	5	60
2017 June	79	7	86
2017 May	94	8	102
2017 April	81	19	100
2017 March	80	11	91
2017 February	55	10	65
2017 January	47	10	57
2016 December	55	12	67
2016 November	52	12	64
2016 October	62	10	72
2016 September	81	18	99
2016 August	67	21	88
2016 July	42	19	61
2016 June	0	18	18
2016 May	2	20	22
2016 April	1	33	34
2016 March	2	37	39
2016 February	1	0	1
2016 January	1	21	22
2015 December	14	15	29
2015 November	74	18	92
2015 October	81	16	97
2015 September	58	13	71
2015 August	57	12	69
2015 July	59	15	74
2015 June	46	8	54
2015 May	57	9	66
2015 April	46	12	58
2015 March	48	11	59
2015 February	49	9	58
2015 January	43	8	51
2014 December	62	15	77
2014 November	42	11	53
2014 October	50	12	62
2014 September	54	20	74
2014 August	53	20	73
2014 July	66	24	90
2014 June	87	18	105
2014 May	105	16	121
2014 April	171	20	191

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